The Jane Coffin Childs Memorial Fund for Medical Research (JCC Fund) was established by the Childs Family in 1937, to honor the memory of Jane Coffin Childs. Inspired by the founding purpose to support research into the causes and treatment of cancer, the Fund’s mission has broadened to support fundamental scientific research that advances our understanding of the causes, treatments, and cures for human disease.

Jane Coffin Childs announces 2025 Jane Coffin Childs Fellows!

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1700

1700 fellows have been funded since the JCC Fund's inception

23

Former fellows & scientific advisors include 23 Nobel laureates

You

Have a chance to be one of the funded. Apply now!

From the blog

2026 Annual Symposium

The Jane Coffin Childs Fund for Medical Research convened in sunny Seattle at the end of April for the 2026 Annual Symposium. JCC fellows, advisors, alumni, and staff gathered on the idyllic shore of the […]

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Featured Fellow

Xinyu Ling, Ph.D.

Xinyu Ling, Ph.D.

Broad Institute of MIT and Harvard

Transposable elements (TEs) play a crucial role in genomic regulation by affecting gene functions, particularly in alternative splicing (AS). Among these, intronic TEs are notably abundant in the human genome, numbering over a million instances. Current research has predominantly fixated on individual TEs near splicing sites, neglecting the vast majority of deep intronic TEs. This oversight hampers our understanding of their collective impact on AS and their relevance to developmental and disease phenotypes. To address this gap, we first start with examining the interaction of TEs within the TBXT gene. TBXT is vital in embryonic development and implicated in tail loss in hominoids and chordoma, a bone cancer where TBXT is aberrantly activated. Exploring these interactions will deepen our knowledge of AS regulation and provide insights into personalized cancer treatment by identifying new genetic markers and therapeutic targets. This research seeks to provide a novel framework to study how the interaction between TEs can affect gene function by modulating pre-mRNA splicing. By uncovering the intricacies of TE-induced AS, we seek to unearth new genetic markers and therapeutic targets, offering novel avenues in disease treatment and prevention.


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